Three-dimensional changes in left and right ventricular geometry in chronic mitral regurgitation. Young, Alistair A., Roger Orr, Bruce H. Smaill, Louis J. Dell'italia. Department of Physiology, [tilde]n Department of Anatomy with Radiology, School of Medicine, University of Auckland, Private Bag 92019, Auckland, New Zealand, [acute]a Birmingham Veteran Affairs Medical Center, University of Alabama at Birmingham, Department of Medicine, Division of Cardiology, University Station, Birmingham, Alabama 35294 and Auburn University College of Veterinary Medicine, Auburn, Alabama 36849-5525
APStracts 3:0278H, 1996.
Regional three dimensional (3D) right and left ventricular geometry was studied in eight dogs before, and five to six months after, induction of mitral regurgitation (MR). Ventricular shape changes were quantified using a 3D finite element model fitted to chamber contours traced on cardiac magnetic resonance images. MR increased LV EDV (99 vs 57 ml, p&LT0.001) and LV stroke volume (SV) (55 vs 26 ml, p &LT 0.001). In contrast, right ventricular EDV decreased (45 vs 55 ml, p &LT 0.01) while SV was maintained. LV mass (free wall plus septum) increased (115 vs 94 g, p&LT0.05), whereas RV free wall mass was relatively unchanged. Shape changes due to MR were characterized by a marked (7.4 mm) rightward shift of the septum relative to the lateral LV free wall at end-diastole. In contrast, the distance from RV free wall to lateral LV free wall was relatively unchanged (2.7 mm). The distance between the LV lateral free wall and septum increased more than the distance between the anterior and posterior LV walls (22% vs 15%, p=0.04). During systole, the displacement of the septum into the LV increased significantly (7.3 vs 2.9 mm, p &LT 0.01). Consistent with the end-diastolic dimension changes, LV endocardial circumferential curvature was decreased at end-diastole to a greater extent in anterior and posterior walls than in septal and lateral walls (p&LT0.01). Thus, chronic MR produced an asymmetric LV dilatation with regional variation in geometry. The septum increased its contribution to the LV SV at the expense of RV EDV. RV SV was maintained, possibly by ventricular interaction.

Received 30 October 1995; accepted in final form 5 June 1996.
APS Manuscript Number H1015-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996